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Effects of ethmozin on sodium current in isolated single ventricular cells were studied using a giga-ohm seal patch electrode and whole cell clamp technique. The results were quite similar with the previous paper on multiple ventricular cell preparation. Further evidences were used to clarify the uncertainty in the previous work of using conventional microelectrode to record action potential. Ethmozin (1-5 mg/L) suppressed phase 0 of action potential recorded in single cell without significant influence on other portions of action potential, which was shown in current clamp mode. In voltage clamp mode, suppress of sodium current (INa) by ethmozin could be recorded through all the physiological voltage range with slight shift of peak (INa) to the positive voltage. Time course of decay of INa was also slowed down by ethmozin. Thus, the mechanism of the slowing down of the rising phase and propagation velocity as well as a rise in threshold of excitability in ventricular muscle reported before was disclosed. Furthermore, ethmozin modified recovery course of INa by decelerating it, which confirmed its use-dependent action discovered before. However, ethmozin promotes its block effect on INa with tonic block stronger than phasic block. Ethmozin has no influence on other membrane current components such as slow inward calcium current and outward potassium current in the present doses. It was concluded that ethmozin is a specified sodium blocker with modification actions on its gating process.